What is the role of the Virchow triad in the pathogenesis of deep venous thrombosis (DVT)?

Venous stasis can occur as a result of anything that slows or obstructs the flow of venous blood. This results in an increase in viscosity and the formation of microthrombi, which are not washed away by fluid movement; the thrombus that forms may then grow and propagate. Endothelial (intimal) damage in the blood vessel may be intrinsic or secondary to external trauma. It may result from accidental injury or surgical insult. A hypercoagulable state can occur due to a biochemical imbalance between circulating factors. This may result from an increase in circulating tissue activation factor, combined with a decrease in circulating plasma antithrombin and fibrinolysins.

Over time, refinements have been made in the description of these factors and their relative importance to the development of venous thrombosis. The origin of venous thrombosis is frequently multifactorial, with components of the Virchow triad assuming variable importance in individual patients, but the end result is early thrombus interaction with the endothelium. This interaction stimulates local cytokine production and facilitates leukocyte adhesion to the endothelium, both of which promote venous thrombosis. Depending on the relative balance between activated coagulation and thrombolysis, thrombus propagation occurs.

Useche JN, de Castro AM, Galvis GE, Mantilla RA, Ariza A. Use of US in the evaluation of patients with symptoms of deep venous thrombosis of the lower extremities. Radiographics. 2008 Oct. 28(6):1785-97. [Medline].

Johnson BF, Manzo RA, Bergelin RO, Strandness DE Jr. Relationship between changes in the deep venous system and the development of the postthrombotic syndrome after an acute episode of lower limb deep vein thrombosis: a one- to six-year follow-up. J Vasc Surg. 1995 Feb. 21(2):307-12; discussion 313. [Medline].

Johnson BF, Manzo RA, Bergelin RO, Strandness DE Jr. The site of residual abnormalities in the leg veins in long-term follow-up after deep vein thrombosis and their relationship to the development of the post-thrombotic syndrome. Int Angiol. 1996 Mar. 15(1):14-9. [Medline].

[Guideline] Qaseem A, Snow V, Barry P, et al for the Joint American Academy of Family Physicians/American College of Physicians Panel on Deep Venous Thrombosis/Pulmonary Embolism. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Fam Med. 2007 Jan-Feb. 5(1):57-62. [Medline]. [Full Text].

Deep venous thrombosis (DVT). There is a substantial mortality benefit for fibrinolytic therapy compared to anticoagulation in patients with right ventricular strain from pulmonary embolism (Konstantinides, 1997).

Deep venous thrombosis (DVT). These sequential images demonstrate treatment of iliofemoral DVT due to May-Thurner (Cockett) syndrome. Far left: View of the entire pelvis reveals iliac occlusion. Middle left: After 12 hours of catheter-directed thrombolysis, an obstruction at the left common iliac vein is evident. Middle right: After 24 hours of thrombolysis, a bandlike obstruction is seen; this is the impression made by the overlying right common iliac artery. Far right: After stent placement, the image shows wide patency and rapid flow through the previously obstructed region. Note that the patient is in the prone position in all views. (Right and left are reversed.)

Deep venous thrombosis (DVT). This lower-extremity venogram shows outlining of an DVT in the popliteal vein with contrast enhancement.

Deep venous thrombosis (DVT). The lower-extremity venogram reveals a nonocclusive chronic thrombus. The superficial femoral vein (lateral vein) has the appearance of two parallel veins, when in fact it is one lumen containing a chronic linear thrombus. Although the chronic clot is not obstructive after it recanalizes, it effectively causes the venous valves to adhere in an open position, predisposing the patient to reflux in the involved segment.

Deep venous thrombosis (DVT). Two views of a commercially available thrombectomy device are shown. The Helix Clot Buster works by creating a vortex with a spinning self-contained propeller that macerates the clot. No thrombolytic agent (ie, tissue plasminogen activator) is necessary when this device is used, but adjunct thrombolytic medications can be useful. Competing devices are available from other manufacturers.

Deep venous thrombosis (DVT). Popliteal vein thrombosis with normal compression of the common femoral vein is demonstrated. Image courtesy of Very Special Images with permission from Dr Lennard A Nadalo.

Deep venous thrombosis (DVT). Bilateral popliteal vein thrombosis with normal compression of the superficial femoral vein is shown. Image courtesy of Very Special Images with permission from Dr Lennard A Nadalo.

Deep venous thrombosis (DVT). Popliteal vein thrombosis is depicted by a Duplex sonogram showing absent flow. Image courtesy of Very Special Images with permission from Dr Lennard A Nadalo.

Deep venous thrombosis (DVT). This contrast-enhanced study was obtained through a Mediport placed through the chest wall through the internal jugular vein to facilitate chemotherapy. A thrombus has propagated peripherally from the tip of the catheter in the superior vena cava into both subclavian veins.

Deep venous thrombosis (DVT). The high-probability perfusion lung scan shows segmental perfusion defects in the right upper lobe and subsegmental perfusion defects in right lower lobe, left upper lobe, and left lower lobe.

Deep venous thrombosis (DVT). A normal ventilation scan will make the defects noted in the previous image a mismatch and, hence, a high-probability ventilation-perfusion scan.

Deep venous thrombosis (DVT). Anterior views of perfusion and ventilation scans are shown. A perfusion defect is present in the left lower lobe, but perfusion to this lobe is intact, making this a high-probability scan.

Deep venous thrombosis (DVT). This sequence of colored digitized pulmonary angiograms (x-ray) in the front view of the pulmonary arteries in a 43-year-old male patient after a heart attack (cardiac arrest) reveals the presence of a pulmonary embolism with a massive thrombus (clot, dark) in the right and left pulmonary arteries. An outline of the lungs are seen. Image courtesy of Science Source/Zephyr.

Deep venous thrombosis (DVT). Hematoxylin and eosin stain. This is a low-power view of a thrombus composed of platelets, fibrin, and leukocytes.

Hearns W Charles, MD Assistant Professor of Radiology, New York University School of Medicine; Attending Physician, Division of Vascular and Interventional Radiology, Department of Radiology, New York University Medical Center

Editions

encoded search term (What is the role of the Virchow triad in the pathogenesis of deep venous thrombosis (DVT)?) and What is the role of the Virchow triad in the pathogenesis of deep venous thrombosis (DVT)?